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GlauCap® is a nutritional supplement developed in close collaboration with ophthalmologists.
It combines CDP-choline, CoQ10 and Nicotinamide and 17 additional micronutrients in a multimodal approach targeting seven neuroprotective mechanisms.
GlauCap® offers a high degree of dosing flexibility. Intake can be individually adjusted according to nutritional status, health conditions, and the specific needs of the person concerned. Capsules should be swallowed whole with sufficient liquid, preferably with a meal. Morning or midday intake is recommended.
An initial phase with a higher daily dose is advised at the start to support a rapid and consistent supply of the contained micronutrients.
Once a stable nutrient level has been achieved, the daily dose can be gradually reduced and individually adjusted.
The following scheme provides a recommended guideline.
Phase | Duration | Capsules per Day |
|---|---|---|
Phase I | 3 – 6 months | 4 capsules |
Phase II | 3 – 6 months | 3 capsules |
Phase II | thereafter | 2 capsules |
Das dargestellte Einnahmeschema dient als Orientierung. Dosierung und Dauer der Einnahme können und sollen entsprechend dem individuellen Krankheitsbild, der Begleittherapie sowie der Verträglichkeit durch Sie angepasst werden.
Did you know that healthcare professionals can request free GlauCap® samples?
„Das weite Feld der Neuroprotektion im Rahmen der Glaukomerkrankung zeigt mit der Entwicklung von neurotrophen, antioxidativen, antiexzitotoxischen, antiischämischen, antiinflammatorischen, antiapoptotischen und immunmodulatorischen Therapieansätzen vielversprechende Fortschritte, die Neurodegeneration zu vermindern und somit die Sehfunktion zu stabilisieren“.
* Anteil der Referenzmenge (Nährstoffbezugswerte = Nutrient Reference Values = NRV) für die tägliche Zufuhr in Prozent nach EU-Verordnung 1169/2011
** keine Nährstoffbezugswerte vorhanden/keine Empfehlung der EU vorhanden
+ Retinoläquivalent (RE)
++ alpha-Tocopheroläquivalent (α-TE)
glutenfrei + lactosefrei
To appreciate the potential benefits of the micronutrients in GlauCap®, it is first important to understand the key neurodegenerative mechanisms in the eye. The following section describes the interplay of oxidative stress, neuroinflammation, and intraocular pressure, providing context for the 7 mechanisms of neuroprotection described afterward.
Even in the early stages of neurodegenerative damage, metabolic and oxidative stress occurs in the unmyelinated axons of retinal ganglion cells. Oxidative stress and mitochondrial dysfunction are closely linked and can trigger neuroinflammation and neurodegeneration. Both mitochondrial and cellular membranes are damaged in the process, ultimately resulting in the death of ganglion cells.
These neurodegenerative processes may occur partly independently of intraocular pressure (IOP); however, they can also affect IOP regulation through changes in the trabecular meshwork. The trabecular meshwork is constantly exposed to oxidative stress, which can be exacerbated by light exposure, metabolic processes, or inflammation. The resulting reactive oxygen species (ROS) damage trabecular cells and alter the extracellular matrix, leading to structural remodelling that impedes aqueous humour outflow and consequently increases intraocular pressure.
Marked fluctuations in IOP, as well as chronically elevated IOP, further increase stress on ganglion cells, thereby promoting progressive neurodegeneration.
The human body relies on complex, intrinsic strategies to protect nerve cells and preserve their function. Targeted nutritional supplementation with GlauCap® can support these mechanisms:
Oxidative stress can damage cell membranes, mitochondria and other sensitive neuronal structures, thereby impairing signal transmission and contributing to neuronal cell death in the long term. The trace elements zinc, selenium and copper, as well as vitamins B2 and C, contribute to the protection of cells from oxidative stress.
An intact cell membrane ensures the structure and stability of cells and is essential for the transmission of nerve impulses. In addition, intracellular membranes—particularly those of mitochondria—play a crucial role in maintaining cellular integrity and function.
Lecithin provides phospholipids such as phosphatidylcholine, a key component of the lipid bilayer of all cell and organelle membranes.
Citicoline supplies essential building blocks for the synthesis and repair of membrane phospholipids.
Vitamin E acts as an antioxidant within membranes, protecting delicate membrane lipids from oxidative stress.
Citicoline and phosphatidylcholine provide the building blocks for the synthesis of the neurotransmitter acetylcholine, which is required for signal transmission between nerve cells1, 2.
Vitamins B1, B3, B6, B12, and C, as well as the trace element copper, contribute to the normal functioning of the nervous system. Zinc contributes to the maintenance of normal cognitive function.
Mitochondria are the central organelles of oxidative phosphorylation and are therefore crucial for providing cellular energy in the form of adenosine triphosphate (ATP). The structural integrity of mitochondrial membranes is essential for the function of the respiratory chain and the maintenance of the electrochemical gradient.
Coenzyme Q10 is an essential component of the mitochondrial respiratory chain. Without Q10, ATP production is significantly impaired. In addition, as a lipophilic antioxidant, Q10 helps stabilise mitochondrial membranes by protecting membrane lipids from oxidative damage, thereby preserving the structural integrity of the mitochondria³.
Vitamin B3 acts as a cofactor in key metabolic processes within the mitochondria and, together with vitamins B1, B2, B6, B12, vitamin C, and copper, contributes to normal energy metabolism.
Blood vessels play a central role in supplying nerve cells with oxygen and micronutrients, as well as in the removal of metabolic waste products. Vessel walls are primarily composed of collagen, which provides both stability and elasticity, allowing the vessels to expand or contract as required. Vitamin C contributes to normal collagen formation, supporting the maintenance of normal vascular function.
Nitric oxide (NO) is an important regulator of blood vessels: it dilates them, thereby improving blood flow and, consequently, the supply of oxygen and nutrients to nerve cells. NO is produced in the body, among other ways, from the amino acid L-arginine⁴.
Vitamins A, B6, folate, B12, and C, as well as the trace elements copper, zinc, and selenium, contribute to the normal functioning of the immune system.
Secondary plant compounds, such as curcuminoids from curcuma and anthocyanins from bilberries, may provide an additional supportive effect. Scientific studies have described their anti-inflammatory and antioxidant properties5-8.
Elevated homocysteine levels (hyperhomocysteinaemia) constitute a significant pathophysiological risk factor for neurodegenerative processes. Homocysteine exerts both direct neurotoxic effects and indirect effects via vascular dysfunction, thereby contributing substantially to neuronal degeneration.
At the neuronal level, homocysteine exerts excitotoxic effects through interactions with glutamatergic receptors, resulting in pathological influx of Ca²⁺ and subsequent intracellular calcium accumulation. Disrupted calcium homeostasis triggers a self-perpetuating cycle of mitochondrial dysfunction and oxidative stress.9-12
Elevated cytosolic calcium concentrations further increase calcium levels within the mitochondrial matrix, impairing electron transport and reducing ATP production, while simultaneously promoting the generation of reactive oxygen species (ROS).
Free ROS damage membrane lipids, mitochondrial proteins, and mitochondrial DNA, causing mitochondria to swell osmotically, take up excess water, and ultimately rupture.
Concurrently, increased oxidative stress induces lipid peroxidation of the cellular membrane, resulting in membrane destabilisation.
Excess cytosolic calcium also provokes endoplasmic reticulum (ER) stress.
Depending on the severity of cellular injury, apoptotic signalling pathways may be activated. In cases of extensive mitochondrial dysfunction, neuronal necrosis is induced.
In addition to its direct neurotoxic effects, homocysteine exerts vasculotoxic effects. It induces endothelial dysfunction via oxidative inactivation of nitric oxide (NO), promotes pro-inflammatory signalling pathways, and fosters a prothrombotic vascular environment.13 The resulting microcirculatory disturbances and chronic hypoperfusion exacerbate neuronal stress and further accelerate neurodegenerative processes.
Vitamins B6, B12, and folate support normal homocysteine metabolism and thereby contribute to neuronal health and vascular function.
References:
1. Adibhatla, R. M., Hatcher, J. F. & Dempsey, R. J. Citicoline: neuroprotective mechanisms in cerebral ischemia.
J. Neurochem. 80, 12–23 (2002).
2. Blusztajn, J. K., Liscovitch, M., Mauron, C., Richardson, U. I. & Wurtman, R. J. Phosphatidylcholine as a precursor of choline for acetylcholine synthesis.
J. Neural Transm. Suppl. 24, 247–59 (1987).
3. Ernster, L. & Dallner, G. Biochemical, physiological and medical aspects of ubiquinone function.
Biochimica et Biophysica Acta – Molecular Basis of Disease 1271, 195–204 (1995).
4. Siasos, G., Tousoulis, D., Antoniades, C., Stefanadi, E. & Stefanadis, C. L-Arginine, the substrate for NO synthesis: An alternative treatment for premature atherosclerosis?
International Journal of Cardiology 116, 300–308 (2007).
5. Abrahams, S., Haylett, W. L., Johnson, G., Carr, J. A. & Bardien, S. Antioxidant effects of curcumin in models of neurodegeneration, aging, oxidative and nitrosative stress: A review.
Neuroscience 406, 1–21 (2019).
6. Hu, S. et al. Clinical development of curcumin in neurodegenerative disease.
Expert Review of Neurotherapeutics 15, 629–637 (2015).
7. Chen, Y. et al. Changes in expression of inflammatory cytokines and ocular indicators in pre-diabetic patients with cataract.
BMC Ophthalmol. 25, 119 (2025).
8. Zaa, C. A., Marcelo, Á. J., An, Z., Medina-Franco, J. L. & Velasco-Velázquez, M. A. Anthocyanins: Molecular Aspects on Their Neuroprotective Activity.
Biomolecules 13 (2023).
9. Verma, M., Wills, Z. & Chu, C. T. Excitatory dendritic mitochondrial calcium toxicity.
Frontiers in Neuroscience 12 (2018).
10. Washington, J., Ritch, R. & Liu, Y. Homocysteine and Glaucoma.
Int. J. Mol. Sci. 24, 10790 (2023).
11. Ganapathy, P. S. et al. Homocysteine-mediated modulation of mitochondrial dynamics in retinal ganglion cells.
Invest. Ophthalmol. Vis. Sci. 52, 5551–5558 (2011).
12. Ho, P. I., Ortiz, D., Rogers, E. & Shea, T. B. Multiple aspects of homocysteine neurotoxicity.
J. Neurosci. Res. 70, 694–702 (2002).
13. Gröber, U. Metabolisches Syndrom–Homocystein als vaskulärer Risikofaktor.
Zeitschrift für Orthomolekulare Medizin 17, 4–5 (2019).
This supplement has been awarded the SUPPLEMENT CERTIFIED seal – an independent, science-backed certification confirming product activity and stability in accordance with label claims.
Our quality standards go well beyond the legal requirements for dietary supplements. Through continuous quality control, strict validation processes, and recognised certifications, we ensure that eye care professionals can confidently recommend safe and reliable micronutrient formulations.
Supplement Certified represents the highest level of verification: an independent, science-supported, and ISO-accredited mark of credibility and quality.
All video contributions from the symposium are availble to view here
Prof. Dr. med. Verena Prokosch
Prof. Dr. med. Stephanie Joachim
Prof. Dr. med. Carl Erb
Prof. Dr. Dr. Thomas Fuchsluger (Chair)
Prof. Dr med Carl Erb, a renowned glaucoma specialist, has been consecutively recognised eight times by FOCUS magazine as one of Germany’s top physicians. In 2019, he was additionally honoured as a specialist in glaucoma. Since 2011, Prof. Erb has served as the leading glaucoma expert at Klinik am Wittenberg Platz in Berlin, Germany. He has also held the position of Vice President of the Glaucoma Section of the German Ophthalmological Society since 2010.
The underlying cause of primary open-angle glaucoma has not yet been fully elucidated, but it is now understood to be a systemic neurodegenerative disease. Since lowering intraocular pressure does not halt disease progression in all patients, complementary therapeutic approaches are being explored. Prof. Dr Carl Erb highlights the importance of nutrition and lifestyle. The full interview with Eyefox can be read here.
Dr. Ghazi Bou Ghanem and Dr. David J. Calkins emphasise that the current clinical focus on managing intraocular pressure (IOP) fails a substantial proportion of glaucoma patients, many of whom continue to progress toward blindness. They argue for a paradigm shift toward a multi-pronged therapeutic strategy that actively supports, protects, and potentially repairs retinal ganglion cells (RGCs) and the optic nerve.
Such neuroprotective strategies may include:
All approaches are explored in detail in their publication, “Addressing Neurodegeneration in Glaucoma: Mechanisms, Challenges, and Treatments,” in Progress in Retinal and Eye Research (Volume 100, May 2024, 101261): https://lnkd.in/eJXFbarf
Through the distribution of samples, ebiga-VISION aims to provide you with the opportunity to experience our products firsthand, enabling you to advise your patients comprehensively and efficiently, and to offer them an evidence-based option.
Please contact us via our contact form. We will be pleased to send you a PDF with our current prices and discount tiers for practice shop operators. Orders can also be placed easily by telephone.
In most countries, patients can order GlauCap® from pharmacies or trusted online retailers. It is also available through the manufacturer’s online shop on the ebiga-VISION website.
